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A developmental switch coupled to the evolution of plasticity acts through a sulfatase

机译:通过硫酸酯酶作用,与可塑性演化相关的发育转换

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Developmental plasticity has been suggested to facilitate phenotypic diversity, but the molecular mechanisms underlying this relationship are little understood. We analyzed a feeding dimorphism in Pristionchus nematodes whereby one of two alternative adult mouth forms is executed after an irreversible developmental decision. By integrating developmental genetics with functional tests in phenotypically divergent populations and species, we identified a regulator of plasticity, eud-1, that acts in a developmental switch. eud-1 mutations eliminate one mouth form, whereas overexpression of eud-1 fixes it. EUD-1 is a sulfatase that acts dosage dependently, is necessary and sufficient to control the sexual dimorphism of feeding forms, and has a conserved function in Pristionchus evolution. It is epistatic to known signaling cascades and results from lineage-specific gene duplications. EUD-1 thus executes a developmental switch for morphological plasticity in the adult stage, showing that regulatory pathways can evolve by terminal addition of new genes.
机译:已建议发育可塑性促进表型多样性,但这种关系的分子机制尚不清楚。我们分析了Pristionchus线虫的进食二态性,由此在不可逆的发育决定后执行了两种成人口型中的一种。通过在表型上不同的种群和物种中将发育遗传学与功能测试相结合,我们确定了可塑性调节剂eud-1,它在发育转换中起作用。 eud-1突变消除了一种嘴形,而eud-1的过表达修复了它。 EUD-1是一种硫酸酯酶,其剂量依赖性地起作用,对于控制喂养形式的性二态性是必要且充分的,并且在Pristionchus进化中具有保守的功能。它对已知的信号级联反应是上位的,并且是由谱系特异性基因重复产生的。因此,EUD-1在成年阶段执行了形态可塑性的发育转换,表明调节途径可以通过末端添加新基因来进化。

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